Protocol to measure acute cerebrovascular and ventilatory responses to isocapnic hypoxia in humans

Kolb, Jon C.; Ainslie, Philip N.; Ide, Kojiro; Poulin, Marc J.

doi:10.1016/j.resp.2004.04.014

Cited by 46 publications

(29 citation statements)

References 18 publications

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“…In addition, an increased CBF caused by an elevation of TPR and MAP combined with an increase in P CO 2 leading to cerebral vasodilatation may serve as a physiological explanation of the observed time delay between decreasing cerebral rSO 2 and SpO 2 values following apnea. The influence of increased arterial P CO 2 is further supported by experiments under hyperoxic conditions with increased inspiratory P CO 2 (7.5 mmHg) leading to elevated CBF in test subjects [33]. Increased CBF should in theory lead to a lower arterial-venous oxygen saturation difference (avDO 2 ), visible as higher cerebral rSO 2 values.…”

Section: Discussionmentioning

confidence: 84%

Evaluation of near-infrared spectroscopy under apnea-dependent hypoxia in humans

Eichhorn

Erdfelder

Kessler

et al. 2015

J Clin Monit Comput

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In this study we investigated the responsiveness of near-infrared spectroscopy (NIRS) recordings measuring regional cerebral tissue oxygenation (rSO2) during hypoxia in apneic divers. The goal was to mimic dynamic hypoxia as present during cardiopulmonary resuscitation, laryngospasm, airway obstruction, or the "cannot ventilate cannot intubate" situation. Ten experienced apneic divers performed maximal breath hold maneuvers under dry conditions. SpO2 was measured by Masimo™ pulse oximetry on the forefinger of the left hand. NIRS was measured by NONIN Medical's EQUANOX™ on the forehead or above the musculus quadriceps femoris. Following apnea median cerebral rSO2 and SpO2 values decreased significantly from 71 to 54 and from 100 to 65%, respectively. As soon as cerebral rSO2 and SpO2 values decreased monotonically the correlation between normalized cerebral rSO2 and SpO2 values was highly significant (Pearson correlation coefficient = 0.893). Prior to correlation analyses, the values were normalized by dividing them by the individual means of stable pre-apneic measurements. Cerebral rSO2 measured re-saturation after termination of apnea significantly earlier (10 s, SD = 3.6 s) compared to SpO2 monitoring (21 s, SD = 4.4 s) [t(9) = 7.703, p < 0.001, r(2) = 0.868]. Our data demonstrate that NIRS monitoring reliably measures dynamic changes in cerebral tissue oxygen saturation, and identifies successful re-saturation faster than SpO2. Measuring cerebral rSO2 may prove beneficial in case of respiratory emergencies and during pulseless situations where SpO2 monitoring is impossible.

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Section: Discussionmentioning

confidence: 84%

Evaluation of near-infrared spectroscopy under apnea-dependent hypoxia in humans

Eichhorn

Erdfelder

Kessler

et al. 2015

J Clin Monit Comput

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“…The participant then began a 3 min baseline walking in normoxia, after which hypoxic breathing was started. The duration of each hypoxic step (3 min) was chosen to ensure enough time for the adjustment of gas mixture and for the measured variables to settle to a new level of P I o 2 , based on 6 x the time constant (s) for rate of oxygen uptake ( _ VO 2 ) and heart rate of *30 s. At the same time, a total hypoxic duration < 20 min was chosen to minimize possible hypoxic ventilatory decline during longer exposures (Kolb et al, 2004).…”

Section: Exercise-hypoxia Protocolmentioning

confidence: 99%

Ventilatory Chemosensitivity, Cerebral and Muscle Oxygenation, and Total Hemoglobin Mass Before and After a 72-Day Mt. Everest Expedition

Cheung

Mutanen²,

Karinen³

et al. 2014

High Altitude Medicine & Biology

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, cerebral and muscle oxygenation, and total hemoglobin mass before and after a 72-day Mt. Everest expedition. High Alt Med Biol 15:331-340, 2014.-Background: We investigated the effects of chronic hypobaric hypoxic acclimatization, performed over the course of a 72-day self-supported Everest expedition, on ventilatory chemosensitivity, arterial saturation, and tissue oxygenation adaptation along with total hemoglobin mass (tHb-mass) in nine experienced climbers (age 37 -6 years, _ VO 2peak 55 -7 mL$kg). Methods: Exercise-hypoxia tolerance was tested using a constant treadmill exercise of 5.5 km$h -1 at 3.8% grade (mimicking exertion at altitude) with 3-min steps of progressive normobaric poikilocapnic hypoxia. Breath-by-breath ventilatory responses, Spo 2 , and cerebral (frontal cortex) and active muscle (vastus lateralis) oxygenation were measured throughout. Acute hypoxic ventilatory response (AHVR) was determined by linear regression slope of ventilation vs. Spo 2 . PRE and POST (< 15 days) expedition, tHb-mass was measured using carbon monoxide-rebreathing. Results: Post-expedition, exercise-hypoxia tolerance improved (11:32 -3:57 to 16:30 -2:09 min, p < 0.01). AHVR was elevated (1.25 -0.33 to 1.63 -0.38 L$min -1. % -1 Spo 2 , p < 0.05). Spo 2 decreased throughout exercise-hypoxia in both trials, but was preserved at higher values at 4800 m post-expedition. Cerebral oxygenation decreased progressively with increasing exercise-hypoxia in both trials, with a lower level of deoxyhemoglobin POST at 2400, 3500 and 4800 m. Muscle oxygenation also decreased throughout exercisehypoxia, with similar patterns PRE and POST. No relationship was observed between the slope of AHVR and cerebral or muscle oxygenation either PRE or POST. Absolute tHb-mass response exhibited great individual variation with a nonsignificant 5.4% increasing trend post-expedition (975 -154 g PRE and 1025 -124 g POST, p = 0.17). Conclusions: We conclude that adaptation to chronic hypoxia during a climbing expedition to Mt. Everest will increase hypoxic tolerance, AHVR, and cerebral but not muscle oxygenation, as measured during simulated acute hypoxia at sea level. However, tHb-mass did not increase significantly and improvement in cerebral oxygenation was not associated with the change in AHVR.

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“…The response during hypocapnia is altered by a first-order, 250-s time constant. 38 Effects of O 2 and CO 2 on Brain Blood Flow We fit analytical functions as above to data on humans subjected to hypoxia from Shapiro et al, 43 Kolb et al, 26 and Cohen et al 2 and we used the Reivich 35 fitting equation derived from data in rhesus monkeys subjected to hypo-and hypercapnia. The resulting equation is …”

Section: Effects Of O 2 and Co 2 On Cardiac Outputmentioning

confidence: 99%

A Mathematical Model of Human Respiration at Altitude

Wolf

Garner

2007

Ann Biomed Eng

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We developed a mathematical model of human respiration in the awake state that can be used to predict changes in ventilation, blood gases, and other critical variables during conditions of hypocapnia, hypercapnia and these conditions combined with hypoxia. Hence, the model is capable of describing ventilation changes due to the hypocapnic-hypoxia of high altitude. The basic model is that of Grodins et al. [Grodins, F. S., J. Buell, and A. J. Bart. J. Appl. Physiol. 22:260-276, 1967]. We updated the descriptions of (1) the effects of blood gases on cardiac output and cerebral blood flow, (2) acid-base balance in blood and tissues, (3) O2 and CO2 binding to hemoglobin and most importantly, (4) the respiratory-chemostat controller. The controller consists of central and peripheral sections. The central chemoceptor-induced ventilation response is simply a linear function of brain P(CO2) above a threshold value. The peripheral response has both a linear term similar to that for the central chemoceptors, but dependent upon carotid body P(CO2) and with a different threshold and a complex, nonlinear term that includes multiplication of separate terms involving carotid body P(O2) and P(CO2). Together, these terms produce 'dogleg'-shaped curves of ventilation plotted against P(CO2) which form a fan-like family for different values of P(CO2). With this chemical controller, our model closely describes a wide range of experimental data under conditions of solely changes in P(CO2) and for short-term hypoxia coupled with P(CO2) changes. This model can be used to accurately describe changes in ventilation and respiratory gases during ascent and during short-term residence at altitude. Hence, it has great applicability to studying O2-delivery systems in aircraft.

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Protocol to measure acute cerebrovascular and ventilatory responses to isocapnic hypoxia in humans

Cited by 46 publications

References 18 publications

Evaluation of near-infrared spectroscopy under apnea-dependent hypoxia in humans

Evaluation of near-infrared spectroscopy under apnea-dependent hypoxia in humans

Ventilatory Chemosensitivity, Cerebral and Muscle Oxygenation, and Total Hemoglobin Mass Before and After a 72-Day Mt. Everest Expedition

A Mathematical Model of Human Respiration at Altitude

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